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Osha 2a > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

What is osteoarthritis?

A
  • wear and tear in the synovial joints
  • imbalance between cartilage wearing down and chondrocyte repair leading to structural issues
  • slow onset
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2
Q

What is the pathophysiology behind osteoarthritis?

A
  • chondrocytes release enzymes
  • these break down collagen and proteoglycans
  • exposure of underlying subchondral bone leads to sclerosis
  • reactive remodelling > osteophytes and subchondral cysts
  • joint space lost
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3
Q

What occurs in the joint as OA gets more severe?

A
  • joint space narrows
  • cartilage loss
  • occurrence and growth of osteophytes
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4
Q

What are the causes and risk factors of OA?

A
  • results from genetic factors, overuse, injury
  • RFs: obesity, age, occupation, female, family history
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5
Q

What are the key criteria for diagnosis of OA?

A
  • over 45
  • pain with activity
  • little to no morning stiffness
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6
Q

Which joints are commonly affected in osteoarthritis?

A
  • affects weight bearing joints
  • hip, knee, wrist
  • sacroiliac joints
  • DIPs in hands
  • carpometacarpal joint at base of thumb
  • cervical spine
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7
Q

How does osteoarthritis present?

A
  • joint pain and stiffness worse with activity and at end of day
  • bulky, bony enlargement of joint
  • restricted range of motion
  • crepitus when moving
  • effusions around joint
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8
Q

What signs of OA are seen in the hands?

A
  • Heberden’s (DIP) and Bouchard’s (PIP) nodes
  • squaring at CMC joint
  • weak grip
  • reduced range of motion
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9
Q

What are the signs of OA in the knee?

A
  • occurs in lateral, patellofemoral or medial (most common) compartments
  • occurs without trauma and with slow evolution
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10
Q

What are the 5 key changes seen on X-ray in OA?

A
  • Joint space narrowing
  • Osteophyte formation
  • Subchondral sclerosis
  • Subchondral cysts
  • Abnormalities of bone contour
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11
Q

What is the non-medical management of OA?

A
  • patient advice
  • weight loss: activity and exercise
  • physio, OT, orthotics
  • walking aids: stick/frame
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12
Q

How is OA managed?

A
  • analgesia: paracetamol, NSAIDs (+PPI), opiates
  • intra-articular steroid injection
  • joint replacement last resort
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13
Q

What is systemic sclerosis?

A
  • autoimmune inflammatory and fibrotic connective tissue disease
  • affects skin and internal organs
  • limited cutaneous or diffuse cutaneous
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14
Q

What are the features of limited cutaneous systemic sclerosis?

A
  • Calcinosis
  • Raynaud’s phenomenon
  • oEsophageal dysmotility
  • Sclerodactyly
  • Telangiectasia
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15
Q

What additional problems occur in diffuse systemic sclerosis?

A
  • cardiovascular: htn and coronary artery disease
  • lung: pulmonary htn and fibrosis
  • renal: glomerulonephritis, renal crisis
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16
Q

What is scleroderma?

A
  • hardening of the skin
  • gives shiny, tight appearance without normal folds
  • most notably occurs on hands and face
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17
Q

What is sclerodactyly?

A
  • skin changes in the hands
  • tightening around the joints
  • fat pads on fingers are lost > breaking and ulceration
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18
Q

What is calcinosis and telangiectasia?

A
  • calcinosis: calcium deposits build up under skin (mostly found on fingertips)
  • telangiectasia: small dilated blood vessels in skin - fine, thready appearance
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19
Q

Why does Raynaud’s occur in systemic sclerosis?

A
  • vasoconstriction leads to fingers going white > blue in response to mild cold
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20
Q

Which autoantibodies are found in systemic sclerosis?

A
  • antinuclear antibodies
  • anti-centromere antibodies (limited)
  • anti-Slc-70 antibodies (diffuse)
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21
Q

What is nailfold capillaroscopy?

A
  • where skin meets fingernails is magnified
  • abnormal capillaries, avascular areas and micro-haemorrhages indicate systemic sclerosis
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22
Q

How is systemic sclerosis managed?

A
  • steroids and immunosuppressants
  • Nifedipine for Raynaud’s
  • PPIs and pro-motility meds for GI
  • physiotherapy for healthy joints
  • skin stretching and gentle emollients
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23
Q

What is rheumatoid arthritis?

A
  • autoimmune condition
  • chronic inflammation of synovial lining of joints, tendon sheaths
  • affects multiple symmetrical, peripheral joints
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24
Q

What is the epidemiology of RA?

A
  • 3x more common in women than in men
  • develops in middle age
  • family history increases risk
  • HLA DR1 and HLA DR4 gene
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25
Q

Which antibodies are found in RA?

A
  • Rheumatoid factor (IgM) is an autoantibody which targets IgG
  • Cyclic citrullinated peptide antibodies (anti-CCP)
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26
Q

How does RA present?

A
  • symmetrical distal polyarthropathy
  • pain, swelling and stiffness
  • occurs in small joints of hands and feet
  • systemic: fatigue, weight loss, flu like, muscle ache
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27
Q

Which joints are most commonly affected in RA?

A
  • PIP
  • MCP
  • wrist and ankle
  • metatarsophalangeal joints
  • cervical spine
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28
Q

What signs of RA are seen in the hands?

A
  • Z shaped deformity to thumb
  • swan neck deformity (hyperextended PIP and flexed DIP)
  • Boutonnieres deformity (hyperextended DIP and flexed PIP)
  • ulnar deviation of fingers at knuckle
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29
Q

What investigations are done for RA?

A
  • FBC: anaemia and infection
  • ESR and CRP
  • RF and anti-CCP
  • X-ray of hands and feet
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30
Q

How is RA managed?

A
  • 1st: methotrexate, leflunomide or sulfasalazine
  • methotrexate in combination with folic acid
  • biological therapy can be added (TNF inhibitor)
  • rituximab
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31
Q

What is the pathophysiology of giant cell arteritis?

A
  • no clear margin between media, adventitia and intima
  • narrowed lumen
  • activated immune cells infiltrate vessel wall > damage and vascular smooth muscle cell remodelling
  • leads to weakening and occlusion of vessels
  • leading to ischaemia, infarction, aneurysm
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32
Q

What is the aetiology of vasculitis?

A
  • 1º: idiopathic autoimmune process
  • 2º: drugs, infection, other autoimmune disease
  • immune complex or ANCA mediated
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33
Q

What are types of large vessel arteritis?

A
  • giant cell arteritis
  • Takayasu arteritis
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34
Q

What are type of medium vessel arteritis?

A
  • Kawasaki disease (coronary in children)
  • polyarteritis nodosa (adults)
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35
Q

What are examples of small vessels ANCA +ve vasculitis?

A
  • small arteries, veins
  • microscopic polyangitis
  • Wegner’s (granulomatosis with polyangitis)
  • Churg-Strauss syndrome
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36
Q

What are examples of immune complex mediated small vessel vasculitis?

A
  • IgA vasculitis: Henoch-Schonlein purpura (more commonly in children)
  • Goodpasture’s (anti-GBM)
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37
Q

What is the general presentation of vasculitis?

A
  • purpura: purple non-blanching spots
  • joint and muscle pain
  • peripheral neuropathy
  • renal impairment
  • GI disturbance
  • systemic: fever, weight loss, fatigue
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38
Q

How is vasculitis diagnosed?

A
  • CRP and ESR raised
  • p-ANCA bloods (Churg-Strauss)
  • c-ANCA bloods (Wegner’s)
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39
Q

How is vasculitis managed?

A
  • steroids: oral, IV, nasal, inhaled
  • immunosuppressants: cyclophosphamide, methotrexate, azathioprine, rituximab
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40
Q

What is the epidemiology of giant cell arteritis?

A
  • scandanavian
  • white
  • peak age: 70-80yrs
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41
Q

What is the presentation of giant cell arteritis?

A
  • temporal headache
  • visual problems
  • scalp tenderness (when brushing hair)
  • tongue/jaw claudication
  • tenderness + thickening of temporal artery
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42
Q

What key visual problems occur with giant cell arteritis?

A
  • blurring
  • veiling
  • double vision (diplopia)
  • photopsia
  • amaurosis fugax
  • KEY: irreversible visual loss in one eye
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43
Q

How is giant cell arteritis investigated?

A
  • 1st line: Raised CRP + ESR
  • Gold: temporal artery US or biopsy (may be missed due to skip lesions)
  • PET-CT for extra cranial disease
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44
Q

How is giant cell arteritis managed?

A
  • oral prednisolone (40-60mg/day)
  • IV methylprednisolone
  • gradual reduction of steroid over 12-18 months
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45
Q

Describe polyarteritis nodosa?

A
  • occurs in males and with hep B, age 40-60
  • can cause renal impairment, stroke, MI
  • associated with mottled purple rash: livedo reticularis
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46
Q

How does granulomatosis with polyangitis (Wegner’s) present?

A
  • epistaxis, crusty nasal secretions
  • hearing loss and sinusitis
  • saddle shaped nose due to perforated septum
  • cough, haemoptysis
  • glomerulonephritis
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47
Q

What is myositis and what is the difference between polymyositis and dermatomyositis?

A
  • autoimmune skeletal muscle inflammation and necrosis
  • polymyositis: chronic muscle inflammation
  • dermatomyositis: connective tissue disorder with chronic muscle and skin inflammation
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48
Q

What are the possible causes and epidemiology of myositis?

A
  • underlying malignancy
  • lung, breast, ovarian and gastric cancer
  • affects females with HLA B8 and HLA DR3 gene
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49
Q

What is the importance of CK in myositis?

A
  • creatine kinase: enzyme released in muscle inflammation
  • usually less than 300U/L but is >1000 in disease
  • can also be caused by: rhabdomyolysis, AKI, MI, strenuous exercise
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50
Q

How does myositis present?

A
  • muscle pain, fatigue and weakness
  • bilaterally, affects proximal muscles
  • affects shoulder and pelvic girdle
  • onset over weeks
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51
Q

How does dermatomyositis present?

A
  • Gottron lesions on knuckles, elbows, knees
  • photosensitive erythematous rash (back, shoulders, neck)
  • purple rash on face + eyelids
  • periorbital oedema
  • calcinosis
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52
Q

Which autoantibodies are seen in myositis?

A
  • Anti-Jo-1: polymyositis
  • Anti-Mi-2 antibodies: dermatomyositis
  • Anti-nuclear antibodies: dermatomyositis
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53
Q

How is myositis diagnosed?

A
  • clinical presentation
  • elevated CK + LDH
  • autoantibodies
  • electromyography
  • muscle biopsy is definitive
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54
Q

How is myositis treated?

A
  • 1st line: corticosteroids
  • immunosuppressants (azathioprine)
  • IV immunoglobulins
  • biological therapy (infliximab)
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55
Q

What is ankylosing spondylitis?

A
  • inflammatory condition of the spine causing progressive stiffness and pain
  • part of seronegative spondyloarthropathy conditions
  • relates to HLA B27 gene
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56
Q

How does ankylosing spondylitis present?

A
  • lower back pain and stiffness
  • sacroiliac pain in buttock
  • pain is worse with rest and improves with movement
  • worse at night, improves in morning (30+ mins activity
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57
Q

How is ankylosing spondylitis investigated?

A
  • CRP and ESR raised
  • HLA B27 raised
  • X-ray of spine and sacrum
  • spinal MRI shows bone marrow oedema
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58
Q

What is seen on X-ray of ankylosing spondylitis?

A
  • Bamboo spine
  • squaring of vertebral bodies
  • subchondral sclerosis and erosion
  • Syndesmyophytes (bone growth at ligaments)
  • ossification of ligaments, discs, joints
  • fusion of joints
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59
Q

How is ankylosing spondylitis managed?

A
  • NSAIDs for pain
  • steroids
  • Anti-TNF: etanercept/infliximab
  • Secukinumab (monoclonal antibody against interleukin-17)
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60
Q

What complications is ankylosing spondylitis associated with?

A
  • anterior uveitis
  • enthesitis
  • dactylitis
  • heart block
  • restrictive lung disease
  • aortitis
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61
Q

What is psoriatic arthritis?

A
  • inflammatory arthritis associated with psoriasis
  • occurs in 10-20% of patients with psoriasis
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62
Q

What is arthritis mutilans?

A
  • occurs in phalanxes
  • osteolysis of bones around joints in digits
  • leads to progressive shortening of finger (telescopic)
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63
Q

What are signs of psoriatic arthritis?

A
  • plaques of psoriasis
  • pitting of nails
  • onycholysis
  • dactylitis
  • enthesitis
  • inflamed DIP joints
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64
Q

What X-ray changes are seen in psoriatic arthritis?

A
  • periosititis: thickened and irregular outline of bone
  • ankylosis: joint stiffening
  • osteolysis: destruction of bone
  • dactylitis: appears as soft tissue swelling
  • pencil-in-cup appearance: central erosions of bones causes one to sit in another
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65
Q

How is psoriatic arthritis managed?

A
  • NSAIDs
  • DMARDS: methotrexate
  • Anti-TNF (etanercept, infliximab)
  • Ustekinumab targets interleukin 12 and 23
66
Q

What is reactive arthritis?

A
  • synovitis occurs in joints as reaction to an infective trigger
  • presents as acute monoarthritis usually in lower limb/knee
67
Q

What is the aetiology of reactive arthritis?

A
  • triggered by infection: gastroenteritis, chlamydia
  • c. jejuni, salmonella, shigella
  • linked to HLA B27
68
Q

What is the presentation of reactive arthritis?

A
  • Reiter’s triad: can’t pee, can’t see, can’t climb a tree: urethritis, arthritis, conjunctivitis
  • uveitis
  • enthesitis
69
Q

How is reactive arthritis managed?

A
  • aspiration to exclude septic arthritis
  • NSAIDs
  • Steroid injections into affected joints
  • systemic steroids if multiple affected
70
Q

What is the difference between osteoporosis and osteopenia?

A
  • osteoporosis: reduction in bone density: bone is weaker and more prone to fracture
  • osteopenia: less severe reduction in bone density
71
Q

What are the risk factors for osteoporosis?

A
  • Steroid use
  • Hyperthyroidism
  • Alcohol
  • Thin (low BMI)
  • Testosterone (low)
  • Early menopause
  • Renal/liver failure
  • Erosive/inflammatory bone disease
  • Dietary low calcium
72
Q

What is the epidemiology of osteoporosis?

A
  • older age
  • female
  • post-menopausal
  • oestrogen is protective
73
Q

What is the pathophysiology behind osteoporosis?

A
  • reduction in bone density
  • osteoclast activity is higher than osteoblast activity causing large spaces in brittle bone
  • usually occurs due to trauma or a fall
  • force applied to bone > strength of bone
74
Q

What 2 scoring systems can be used to grade osteoporosis?

A
  • DEXA scan: measures bone mineral density with T score of hip
  • FRAX score: 10 year probability of major osteoporotic fracture
75
Q

Describe DEXA scoring

A
  • Normal: T ≥ -1.0
  • Osteopenia -2.5 < T < -1.0
  • Osteoporosis T ≤ -2.5
  • Severe osteoporosis T ≤ -2.5 plus a fracture
76
Q

How should osteoporosis be investigated?

A
  • FRAX on women > 65 and men > 75, younger patients with risk factors
  • If intermediate risk: offer DEXA, if high then offer treatment
77
Q

How is osteoporosis managed?

A
  • avoiding falls
  • calcium supplementation with vit D
  • glucocorticoids
  • 1st line: bisphosphonates e.g. zoledronic acid
  • 2nd line: Denosumab
78
Q

What lifestyle advice is given for osteoporosis?

A
  • exercise
  • maintain healthy weight
  • stop smoking
  • reduce alcohol
  • avoid falls
79
Q

How do bisphosphonates work and what are the side effects?

A
  • interfere with osteoclasts and reduce their activity
  • prevents reabsorption of bone
  • side effect: osteonecrosis of jaw and auditory canal
  • reflux and oesophageal erosion
80
Q

How does Denosumab work?

A
  • blocks osteoclast activity by binding to the RANK-ligand
81
Q

What is gout?

A
  • crystal arthropathy
  • chronically high blood uric acid levels
  • urate crystals deposition causing hot, swollen, painful joints
82
Q

What is the aetiology of gout?

A
  • high purine foods: beer, shellfish, offal, red meat, fructose
  • low dose aspirin, diuretics and ketones impair renal ability to excrete uric acid
83
Q

What are the risk factors for gout?

A
  • male
  • obesity
  • high purine diet (meat)
  • alcohol
  • existing CVD/renal disease
  • family history
84
Q

How is gout managed acutely?

A
  • 1st line: NSAIDs
  • 2nd line: colchicine
  • 3rd line: steroid
85
Q

How is gout managed in the long-term?

A
  • allopurinol: xanthine oxidase inhibitor which reduces uric acid levels
  • lifestyle changes: losing weight, staying hydrated, minimising consumption of high purine foods
86
Q

What does fluid aspiration from gout show?

A
  • no bacterial growth
  • needle shaped crystals
  • negatively birefringent of polarised light
  • monosodium urate crystals
87
Q

What do joint X-rays in gout show?

A
  • joint space maintained
  • lytic lesions
  • punched out erosions with sclerotic borders and overhanging edges
88
Q

Which joints does gout typically affect?

A
  • base of big toe (metatarso-phalangeal)
  • DIP joints in hands
  • wrist
  • base of thumb
89
Q

How does gout present?

A
  • gouty top: subcut deposits of uric acid
  • affects small joints and connective tissues in hand, ears, elbows
  • single acute hot, swollen, painful joint
90
Q

What is the pathophysiology of gout?

A
  • purines are converted to uric acid by xanthine oxidase
  • it is normally in the form of monosodium urate in the blood
  • most cases occur if there is impaired excretion (kidneys), not from uric acid overproduction
91
Q

What is pseudogout and what is the epidemiology?

A
  • crystal arthropathy caused by calcium pyrophosphate crystals
  • mostly in elderly women
92
Q

What is the pathophysiology behind pseudogout?

A
  • chondrocytes are the main cell involved in formation and deposition of CPP
  • excess pyrophosphate production leads to CPP over saturation
  • the excess CPP takes the form of crystals
  • this stimulates a pro inflammatory response leading to activation of neutrophils and phagocytes
93
Q

How does pseudogout present?

A
  • older adults
  • hot, swollen, stiff, painful knee, shoulder, wrist or hip
  • chronic
  • can be asymptomatic and picked up on X-ray
94
Q

How is pseudogout diagnosed?

A
  • aspiration for synovial fluid
  • calcium pyrophosphate crystals
  • rhomboid shaped
  • positive birefringent of polarised light
95
Q

What is chondrocalcinosis?

A
  • thin white line in the middle of the joint space
  • caused by calcium deposition
  • appears on X-ray
  • Gold standard diagnosis for pseudogout
96
Q

How is pseudogout managed?

A
  • usually resolves spontaneously
  • NSAIDs, colchicine, joint aspiration
  • steroids
  • arthrocentesis if severe
97
Q

What is the key differential diagnosis to be excluded from the crystal arthropathies?

A
  • septic arthritis also presents with an acute, hot, swollen and painful joint
98
Q

What is SLE?

A
  • inflammatory autoimmune connective tissue disease
  • presents with non-specific symptoms
  • relapsing-remitting course
99
Q

What is the epidemiology of SLE?

A
  • more common in:
  • women
  • Asians
  • presents in young to middle aged adults
100
Q

What is the pathophysiology behind SLE?

A
  • characterised by anti-nuclear antibodies
  • antibodies to proteins within the person’s cell nucleus
  • this causes an autoimmune response
101
Q

How does SLE present?

A
  • fatigue
  • weight loss
  • photosensitive malar rash (butterfly shaped across nose and cheeks - worsens with sunlight)
  • shortness of breath
  • lymphadenopathy and splenomegaly
  • glomerulonephritis
  • Raynaud’s
102
Q

What investigations can be done for SLE?

A
  • FBC: normocytic anaemia
  • decreased C3 and C4 levels
  • raised CRP and ESR
  • raised immunoglobulins
  • autoantibodies
103
Q

Which autoantibodies are commonly seen in SLE?

A
  • anti-nuclear antibodies +ve in 85% patients
  • Anti-dsDNA
  • Anti-ENA
104
Q

How is SLE treated?

A
  • 1st line: NSAIDs, corticosteroids, hydroxychloroquine
  • methotrexate, leflunomide, azathioprine
  • avoid sunlight and use suncream
105
Q

What complications can occur from SLE?

A
  • CVD
  • infection
  • anaemia of chronic disease
  • pericarditis or pleuritis
  • lupus nephritis
106
Q

What is antiphospholipid syndrome?

A
  • Blood becomes prone to clotting and patient is in hyper-coagulable state
  • associated with antiphospholipid antibodies
107
Q

The presence of which antibodies are used to diagnose antiphospholipid syndrome?

A
  • lupus anticoagulant
  • anticardiolipin antibodies
  • Anti-β-2 glycoprotein I antibodies
108
Q

What conditions is antiphospholipid syndrome associated with?

A
  • DVT and PE
  • stroke, MI and renal thrombosis
  • miscarriage, stillbirth and pre-eclampsia
  • Libmann-Sacks endocarditis
109
Q

What signs and symptoms are common in antiphospholipid syndrome?

A
  • livedo reticularis: purple lace like rash giving mottled appearance
  • thrombocytopenia
110
Q

How is antiphospholipid syndrome managed?

A
  • long term warfarin with INR range of 2-3
  • pregnant women in LmwH and aspirin
111
Q

What is Sjrogen’s?

A
  • autoimmune condition affecting exocrine glands
  • 1º occurs in isolation, 2º related to SLE/RA
112
Q

Which antibodies are found in Sjrogen’s?

A
  • anti-Ro and anti-La
113
Q

What symptoms are caused by Sjrogen’s?

A
  • leads to dry mucous membranes:
  • dry eyes, mouth, vagina
114
Q

How is Sjrogen’s diagnosed?

A
  • Schirmer test
  • inset folded piece of filter paper under lower eyelid
  • tears should travel 15mm in 5 mins
  • <10mm is significant
115
Q

How is Sjrogen’s managed?

A
  • artificial tears, saliva
  • vaginal lubricants
  • hydroxychloroquine to halt progress
116
Q

What is fibromyalgia?

A
  • non-specific muscular disorder
  • primarily affects insertions of tendons, associated soft tissues
  • potentially hyper excitability of pain fibres
  • more common in women with onset 40-50
117
Q

What is the presentation of fibromyalgia?

A
  • pain worse with stress, cold weather and activity
  • morning stiffness
  • pins and needles in hands and feet
  • poor sleep
118
Q

How is fibromyalgia diagnosed?

A
  • widespread bilateral joint pain above and below the hips
  • pain on > 11 of the 18 palpable sites for at least 3 months
119
Q

How is fibromyalgia managed?

A
  • manage pain: amitriptyline - avoid opioids
  • improve sleep
  • exercise
  • local heat application
120
Q

What are examples of types of bone tumours?

A
  • chondrosarcoma
  • osteosarcoma (in children)
  • Ewing sarcoma (bone marrow)
  • giant cell tumour of bone (benign)
121
Q

What are risk factors for bone tumours?

A
  • previous radiotherapy
  • previous cancer
  • Paget’s disease
  • benign lesions
122
Q

How do bone malignancies present?

A
  • common in long bones
  • worse at night, resistant to analgesia
  • bony/soft tissue swelling
  • easy bruising
  • mobility issues - joint stiffness, reduced range of motion
123
Q

What investigations are done for bone tumours?

A
  • 1st line: X-ray
  • Gold: bone biopsy
  • Bloods: FBC, ESR, Ca, U&Es
124
Q

How are MSK malignancies managed?

A
  • chemo/radiotherapy
  • surgical resection: limb sparing or sacrificing
125
Q

From where do tumours most commonly metastasise to bone?

A
  • Breast (Sclerotic/Mixed)
  • Lung (Lytic / Mixed)
  • Thyroid (Lytic)
  • Kidney (Lytic)
  • Prostate (Sclerotic/Mixed)
126
Q

What is polymyalgia rheumatica?

A
  • inflammatory condition causing pain and stiffness in shoulders, neck and pelvic girdle
  • strong association with giant cell arteritis
127
Q

What is the epidemiology of polymyalgia rheumatica?

A
  • female
  • age 50+
  • more common in caucasians
128
Q

How does PMR present?

A
  • bilateral shoulder pain radiating to elbow
  • bilateral pelvic girdle pain
  • worse with movement and interferes with sleep
  • morning stiffness >45 mins
129
Q

How is PMR diagnosed?

A
  • ESR and CRP raised
  • Bloods: FBC, U&Es, LFTs
  • symptoms lasting 2+ weeks
130
Q

How is PMR treated?

A
  • 15mg prednisolone per day
  • assess after 1 week and 3-4 weeks
  • if symptoms improve start a reducing regime
131
Q

What are the differential diagnoses for PMR?

A
  • myeloma
  • myositis
  • RA/osteoarthritis
  • SLE
  • osteomalacia
  • fibromyalgia
132
Q

What is septic arthritis and what is a common cause?

A
  • infection in native or joint replacement
  • destroys joint and causes systemic illness
  • common complication of hip and knee replacements
133
Q

How does septic arthritis present?

A
  • affects single joint, often knee
  • hot, red, swollen, painful joint
  • stiffness and reduced range of motion
  • systemic: fever, lethargy
134
Q

Which bacteria commonly cause septic arthritis?

A
  • Staph aureus
  • Neisseria gonorrhoea
  • Strep pyogenes
  • Haemophilus influenza
  • E. coli
135
Q

How is septic arthritis investigated?

A
  • joint aspiration
  • gram staining, crystal microscope, culture
  • antibiotic sensitivities
136
Q

How is septic arthritis managed?

A
  • empirical IV antibiotics for 3-6 weeks
  • flucloxacillin + rifampicin
  • vancomycin if allergic to penicillin
137
Q

What is osteomyelitis?

A
  • inflammation in a bone and bone marrow
  • haematogenous: pathogen carried through blood to the bone
  • acute or chronic
  • most commonly caused by Staph aureus
138
Q

What are the risk factors for osteomyelitis?

A
  • open fractures
  • orthopaedic operations
  • diabetes
  • peripheral arterial disease
  • IV drug use
139
Q

How does osteomyelitis present?

A
  • fever
  • pain and tenderness
  • erythema
  • swelling
  • systemic symptoms
140
Q

How is osteomyelitis investigated?

A
  • MRI
  • Bloods: cultures, raised inflammatory
  • bone cultures
141
Q

How is osteomyelitis treated?

A
  • surgical debridement of infected bone and tissue
  • antibiotic therapy: 6 weeks of flucloxacillin ± rifampicin
142
Q

What are potential signs of osteomyelitis on X-ray?

A
  • periosteal reaction (changes to bone surface)
  • localised osteopenia (bone thinning)
  • destruction of areas of bone
143
Q

What is the difference in age and speed of onset between inflammatory and degenerative joint disease?

A
  • Inflammatory: can happen at any age, rapid (weeks-months)
  • Degenerative: usually in later life, slow - years
144
Q

What is the mechanism of action of anti-TNF drugs?

A
  • blocks tumour necrosis factor which is a cytokine that stimulates inflammation
  • infliximab is a monoclonal antibody to TNF
145
Q

What is Paget’s?

A
  • excessive bone turnover due to excess activity of osteoblasts and osteoclasts
  • leads to areas of sclerosis and lysis
  • leads to enlarged and misshapen bones which increase risk of pathological fractures
  • affects axial bones
146
Q

How does Paget’s present?

A
  • bone pain and deformity
  • fractures
  • hearing loss if ear bones affected
147
Q

What does X-ray of someone with Paget’s show?

A
  • bone enlargement and deformity
  • osteoporosis circumscripta: well defined dense lesions
  • cotton wool appearance
  • V-shaped defects in long bones
148
Q

What do bloods for Paget’s show?

A
  • raised ALP
  • normal calcium and phosphate
149
Q

How is Paget’s treated?

A
  • bisphosphonates interfere with osteoclast activity
  • NSAIDs
  • calcium and vit D supplementation
150
Q

What are key complications of Paget’s?

A
  • osteosarcoma
  • spinal stenosis
151
Q

What is the pathology behind mechanical lower back pain?

A
  • damage to the muscles and soft tissues of the back due to posture, physical activity, lifting
  • disorders of the facet joints of the spine
  • muscle spasm > pain > spasm > pain
152
Q

What are the risk factors for chronic lower back pain?

A
  • smoking
  • poor working conditions
  • psychological disorders
  • low socioeconomic status
153
Q

How does mechanical back pain present?

A
  • lower back pain
  • worse on movement (twisting/bending)
  • relieved by rest and at night
  • history of specific injury
154
Q

How is mechanical back pain managed?

A
  • mostly self resolving
  • heat
  • analgesia
  • physiotherapy
  • preventative: weight loss, muscle conditioning
155
Q

From where do tumours most commonly metastasise to bone?

A
  • Breast (Sclerotic/Mixed)
  • Lung (Lytic / Mixed)
  • Prostate (Sclerotic/Mixed)
  • Kidney (Lytic)
  • Thyroid (Lytic)
156
Q

What is osteomalacia?

A
  • defective bone mineralisation causes soft bones
  • results from insufficient vitamin D
157
Q

What is the pathophysiology behind osteomalacia?

A
  • vit D is created from cholesterol by the skin in response to UV radiation
  • it is essential in absorbing calcium and phosphate from the intestines and kidneys
  • low levels lead to defective bone mineralisation
158
Q

How is low vitamin D related to PTH?

A
  • low vit D > low serum calcium
  • this causes 2º hyperparathyroidism
  • parathyroid gland tries to raise calcium level by secreting PTH
  • PTH stimulates increased reabsorption from the bone
159
Q

What is the presentation of osteomalacia?

A
  • fatigue
  • bone pain
  • muscle weakness and aches
  • pathological/abnormal fractures
  • looser zones (partial fragility fractures)
160
Q

What is the investigation of osteomalacia?

A
  • serum 25-hydroxyvitamin D
  • <25 nmol/L: vit D deficiency
  • 25-50nmol/L: vit D insufficiency
  • X-ray shows osteopenia and DEXA shows low density

Osha 2a (15 decks)

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